| Identifier | HPI103492 |
| Interaction | p53 <==> IRF-1 |
| Role & State | RS:0000002,activity; RS:0000077,regulator; |
| Interaction Type | IT:0000372,treatment; IT:0000099,formation; IT:0000114,activation; IT:0000068,transcription; IT:0000078,regulation; |
| Biological Process | BP:0007049,cell cycle; BP:0006281,DNA repair; BP:0006412,translation; BP:0006915,apoptosis; BP:0007050,cell cycle arrest; |
| Biological Function | BF:0016563,transcriptional activity; |
| Subcelluar Location | --- |
| Detection Method | --- |
| Reference | 16832344_0, Single-stranded RNA viruses inactivate the transcriptional activity of p53 but induce NOXA-dependent apoptosis via post-translational modifications of IRF-1, IRF-3 and CREB.
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| Reference | 16832344_3, Transcriptional activation of NOXA by VSV or SV is independent of p53, but requires the presence of interferon regulatory factor 1 (IRF-1), IRF-3 and cAMP-responsive element binding protein (CREB).
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| Reference | 9472983_0, Altered DNA repair and dysregulation of p53 in IRF-1 null hepatocytes.
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| Reference | 9472983_2, In different cell types, IRF-1 and p53 can cooperate to produce cell cycle arrest (embryo fibroblasts) or can independently trigger apoptosis (lymphoid cells). p53 may also regulate DNA repair, but there is no information on IRF-1 and repair.
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| Reference | 9472983_7, Hepatocyte apoptosis after UV treatment, previously reported to be independent of p53, was also independent of IRF-1.
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